ArticleThe Journal of biological chemistry2015
Uncoupling Protein 1 and Sarcolipin Are Required to Maintain Optimal Thermogenesis, and Loss of Both Systems Compromises Survival of Mice under Cold Stress.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Mitochondria-associated regulation in adipose tissues and potential reagents for obesity intervention.Frontiers in endocrinology · 2023Pooled it
- Sarcopenia and body temperature-the significance of interorgan metabolic networks in skeletal muscle atrophy.Endocrine journal · 2026Review
- Cold exposure and human metabolism: A heterogeneous response across tissues and organs.Temperature (Austin, Tex.) · 2026Review
- Sarcolipin-SERCA uncoupling as a plausible heat source for sustaining fever.Frontiers in physiology · 2026Article
- Body Temperature Regulation in the Rat by Muscle Tone.Acta physiologica (Oxford, England) · 2026Article
- Brown adipose tissue and skeletal muscle coordinately contribute to thermogenesis in mice.eLife · 2025Article
- SERCA blockade as a treatment strategy for obesity.European journal of applied physiology · 2025Review
- Physiological Conditions, Bioactive Ingredients, and Drugs Stimulating Non-Shivering Thermogenesis as a Promising Treatment Against Diabesity.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Futile Creatine Cycle powers UCP1-independent thermogenesis in classical BAT.Nature communications · 2025Article
- Adaptive Induction of Nonshivering Thermogenesis in Muscle Rather Than Brown Fat Could Counteract Obesity.Physiological research · 2024Review
- Article
- Adipose Tissue and Metabolic Health.Diabetes & metabolism journal · 2023Review
- CCE and EODF as two distinct non-shivering thermogenesis models inducing weight loss.Pflugers Archiv : European journal of physiology · 2023Article
- Thermogenic Brown Fat in Humans: Implications in Energy Homeostasis, Obesity and Metabolic Disorders.The world journal of men's health · 2023Review
- Article
- Rats lacking Ucp1 present a novel translational tool for the investigation of thermogenic adaptation during cold challenge.Acta physiologica (Oxford, England) · 2023Article
- Pathological bile acid concentrations in chronic cholestasis cause adipose mitochondrial defects.JHEP reports : innovation in hepatology · 2023Article
- Physiological and molecular mechanisms of cold-induced improvements in glucose homeostasis in humans beyond brown adipose tissue.International journal of obesity (2005) · 2023Review
- A single-cell transcriptional timelapse of mouse embryonic development, from gastrula to pup.bioRxiv : the preprint server for biology · 2023Article
- Hypermetabolism in mice carrying a near complete human chromosome 21.bioRxiv : the preprint server for biology · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The importance of brown adipose tissue as a site of nonshivering thermogenesis has been well documented. Emerging studies suggest that skeletal muscle is also an important site of thermogenesis especially when brown adipose tissue function is lacking. We recently showed that sarcolipin (SLN), an uncoupler of the sarco(endo)plasmic reticulum Ca(2+) ATPase (SERCA) pump, could contribute to heat production in skeletal muscle. In this study, we sought to understand how loss of UCP1 or SLN is compensated during cold exposure and whether they are both necessary for thermogenesis. Toward this goal, we generated a UCP1;SLN double knock-out (DKO) mouse model and challenged the single and DKO mice to acute and long-term cold exposures. Results from this study show that there is up-regulation of SLN expression in UCP1-KO mice, and loss of SLN is compensated by increased expression of UCP1 and browning of white adipose tissue. We found that the DKO mice were viable when reared at thermoneutrality. When challenged to acute cold, the DKO were extremely cold-sensitive and became hypothermic. Paradoxically, the DKO mice were able to survive gradual cold challenge, but these mice lost significant weight and depleted their fat stores, despite having higher caloric intake. These studies suggest that UCP1 and SLN are required to maintain optimal thermogenesis and that loss of both systems compromises survival of mice under cold stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.